After 30 years in the doctor trenches, every so often I think about patients I desperately wanted to save—and didn’t. At the top of my list is Arthur Lewis. A quiet, well-mannered teenager, Lewis developed a fungal infection that attacked multiple organs. Three years and many treatments later, the fungus claimed his life.
Most infectious diseases are color-blind; their outcome has nothing to do with their hosts’ hue. But Lewis’s illness, coccidioidomycosis, was different. His African American ancestry put him at special risk for the battle he bravely fought and lost.
His struggle reminds me of a basic truth in medicine. Although excellent care can tip the balance between life and death, in some cases patients have genetic vulnerabilities that all the high-tech care in the world simply cannot conquer. Genes aren’t everything when it comes to coccidioidomycosis, a rare soilborne illness that can be acquired by inhaling dust. Other variables (like the dose of inhaled organisms, underlying lung anatomy, and subtle or overt immune problems) also influence the course of the illness. But genes can gravely color the outcome. Some patients with acute coccidioidomycosis experience a short-lived infection that takes no more of a toll than the flu. In other cases, patients develop a chronic hacking cough, unexplained rashes, and joint pain. Many patients do not require specific treatment, but those who do can have tragically different outcomes.
Before I tell Lewis’s story, I’ll start with another man with the same infection and racial risk—and a happier ending. The year was 1985; the place, Van Nuys, California. A lanky African American in gym shorts and T-shirt practically bounded into the waiting room of the clinic where I worked, his mood and dress worlds apart from our usual clientele. Back then, most of our patients had HIV, tuberculosis, or a complication from IV drug abuse. When we opened our doors at 7:30 a.m., the AIDS sufferers were bundled in sweaters, the TB folks (hard-working immigrants, for the most part) wore everything from painters’ pants to saris, and the drug addicts had not yet arrived.
Through a window I peered at the lively newcomer and wondered: What brings you here, stranger? During my time as the sole infectious-diseases specialist at this small county outpost, no one ever visited our weekly clinic unless they had to. Ten minutes later, in an exam room, we learned Luke Jackson’s reason for coming.
The 34-year-old coach and substitute teacher told us that a month earlier, he had noticed a small crusty patch, roughly the size of a nickel, on his left flank. Lacking health insurance, he consulted our county dermatologist. No, it wasn’t cancer, he was told, and it didn’t look like eczema or psoriasis either. So Jackson agreed to a standard skin biopsy that took five minutes from start to finish, then forgot all about it.
Until a couple of weeks later, that is, when a dermatology clerk called and referred him to me. Something surprising had shown up on his biopsy. “I think she called them…spherules?” Jackson said, wrinkling his brow. “Frankly, Doc, I began to feel like a pod person from Invasion of the Body Snatchers. What the heck is a spherule?”
I imagined Jackson’s spherules—microscopic cysts stuffed with endospores—and realized why the clerk had used this word from the pathology lab report rather than the tongue-twisting term Coccidiodes immitis, the fungus responsible for Jackson’s tiny cluster bombs.
So far, so good. By the time they finished their rotation with me, every resident at my hospital had seen one or two patients with “cocci,” also known as valley fever—a label that harks back to the disease’s early discovery in California’s San Joaquin Valley. There, as in other semiarid pockets of the American Southwest, inhaling spore-laced dust was the usual way that humans (and the occasional pet dog) contracted C. immitis. Small outbreaks sometimes followed windstorms or earthquakes. For example, Ventura County, just north of Los Angeles, reported 203 cases of cocci, three of them fatal, after the January 1994 earthquake centered in Northridge. However, an earthquake was not to blame for Jackson’s infection. As a jogger and trail biker, he was a perfect candidate for ordinary exposure through dust inhalation.
The problem was that his case was far from the classic, quickly forgotten flulike variety. On the contrary, his single skin lesion teeming with cocci spherules confirmed a far more ominous scenario: After silently proliferating in Jackson’s lungs, fungal spores had traveled through his bloodstream and had been deposited in his skin.
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